Neonates Flashcards

1
Q

what cells produce surfactant?

A

type 2 pneumocytes

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2
Q

when are type 2 pneumocytes mature enough to produce surfactant?

A

between 24-34 weeks gestation

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3
Q

what is surface tension?

A

attraction of the molecules in a liquid to each other, pulling them together and minimising surface area

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4
Q

what does surfactant do?

A

reduces surface tension - maximising the surface area of the alveoli and increase compliance

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5
Q

what does the squeezing of the thorax at birth do to the lungs?

A

helps clear fluid from the lungs

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6
Q

what stimulates the first breath of a baby and why is it important?

A

Birth, temperature change, sound and physical touch stimulate the baby to promote first breath

Strong first breath= required to expand previously collapsed alveoli for the first time. Adrenalin and cortisol are released in response to the stress of labour, stimulatory respiratory effort.

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7
Q

how does the first breath lead to the closure of the foramen ovale?

A

first breath = expands alveoli = decreased pulmonary vascular resistance = fall in pressure in RA, = LA pressure higher = functional closure of foramen ovale

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8
Q

what causes the closure of the ductus arteriosus?

A

Prostaglandins keep ductus arteriosus open, increased blood oxygenation causes a drop in circulating prostaglandin

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9
Q

what causes the ductus venosus to close?

A

Immediately after the ductus venosus stops functioning because the umbilical cord is clamped and there is no blood flow in the umbilical veins. The ductus venosus structurally closes a few days later to become ligamentum venosum.

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10
Q

what constitutes very low birth weight and extremely low birth weight?

A

Very low birth weight = <1.5kg
Extremely low birth weight = <1kg

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11
Q

describe the affects of hypoxia in normal labour?

A

Normal labour and birth leads to hypoxia. contractions = placenta is unable to carry out normal gaseous exchange = hypoxia.

Extended hypoxia = anaerobic respiration and bradycardia. Further= reduced consciousness and a drop in respiratory effort, in turn worsening hypoxia.

Extended hypoxia= Hypoxic-ischaemic encephalopathy (HIE), with potentially life changing consequences such as cerebral palsy.

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12
Q

4 issues in neonatal resuscitation

A
  • hypoxia
  • large surface area to weight ratio = get cold easily
  • wet = lose heat rapidly
  • babies born through meconium may have this in mouth/airway
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13
Q

what are the principals of neonatal resuscitation?

A
  • warm the baby
    • get dry asap, heat lamp, <28 weeks in plastic bag under lamp
  • apgar
  • stimulate breathing
    • vigorously dry with towel
    • head in neutral position, check for obstruction
  • inflation breaths
    • given when gasping or not breathing despite adequate stimulation
  • compressions
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14
Q

when is APGAR calculated

A

1, 5, 10 mins after birth

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15
Q

what is the APGAR score?

A
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16
Q

how are inflation breaths given?

A
  • Two cycles of five inhalation breaths (lasting 3 seconds each) can be given to stimulate breathing and heart rate
  • If there is no response and HR low, 3 seconds ventilation breaths can be used
  • If there is still no response, chest compressions can be used, coordinated with the ventilation breaths.

Technique very important.

Air for term or near term babies

mix of air and oxygen in pre-term babies.

O2 sats can be monitored throughout if there are concerns about breathing.

Aim for gradual rise and do not exceed 95%

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17
Q

what is delayed cord clamping?

A

allows for more blood to enter the circulation of the baby.

AKA PLACENTAL TRANSFUSION.

Recent evidence indicated that in healthy babies, delaying Hb= Hb, Iron stores and BP and a reduction in intraventricular haemorrhage and necrotising enterocolitis.

The only apparent negative affect is neonatal jaundice, potentially requiring phototherapy.

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18
Q

what is the current guideline on delayed cord clamping?

A

uncompromised neonates - delay of at least 1 minute following birth

neonates requiring resus - clamped sooner to prevent delays in getting resus

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19
Q

what needs to happen to the baby immediately after birth?

A
  • Skin to skin
  • Clamp the cord
  • Dry the baby
  • Keep the baby warm in hat and blankets
  • VitK
  • Label the baby
  • Measure the weight and length
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20
Q

why are babies given vitamin K shortly after birht?

A

Babies are born with a deficiency of VitK. IM injection in the thigh shortly after birth. Can have a helpful side effect of stimulating the baby to cry, which helps expand the lungs. Vitamin K helps prevent bleeding, particularly intracranial, umbilical stump, and GI bleeding. Alternatively, vitamin K can be given orally, however this takes longer to act and requires doses at birth. 7 days and 6 weeks.

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21
Q

what is the benefit of skin to skin contact?

A
  • Helps warm baby
  • Improves mother and baby interaction
  • Calms baby
  • Improves breastfeeding
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22
Q

when is breast/bottle feeding initiated?

A

as soon as baby is alert enough

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23
Q

when does the newborn examination need to be conducted by?

A

within 72 hours

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24
Q

when is the newborn hearing test conducted and what is it?

A

first 4 to 5 weeks

automated otoacoustic emission (AOAE)

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25
Q

what is the blood spot screening test, what does it test for and when is it done??

A

9 genetic conditions.

Is taken on day 5 (day 8 at the latest) after consent from the parent.

A heel prick is used to provide drops of blood. Screening card requires four separate drops.

  • Sickle cell disease
  • CF
  • Congenital hypothyroidism
  • Phenylketonuria
  • Medium-chain acyl-CoA dehydrogenase deficiency (MCADD)
  • Maple syrup urine disease
  • Isovaleric acidaemia (IVA)
  • Glutaric aciduria type 1 (GA1)

results come back in 6-8 weeks

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26
Q

what is a caput succedaneum?

A

oedema collecting on the scalp - outside the periosteum

caused by pressure to a specific area of the scalp during traumatic, prolonged or instrumental delivery

crosses the suture lines

resolves spontaneously in a few days

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27
Q

what is a cephalohematoma?

A

collection of blood between the skull and periosteum

caused by damaged blood vessels during traumatic, prolonged or instrumental delivery

DOES NOT cross suture line

causes discolouration of skin in selected areas

normally resolves in a few months with no intervention

risk of anaemia and jaundice due to blood collecting within haematoma & breakdown

monitor for anaemia, jaundice and resolution

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28
Q

what is facial paralysis?

A

facial nerve palsy from forceps delivery

normally resolve spontaneously

may require neurosurg input if doesn’t resolve

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29
Q

what is Erb’s Palsy?

A

injury to C5/C6 nerves in brachial plexus during birth

associated with shoulder dystocia, traumatic or instrumental delivery and large birth weight

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30
Q

how does erbs palsy present

A

damage to C5/C6 nerve leads to weakness of shoulder adbuction and external rotation, arm flexion, finger extension

  • waiters tip:
    • Internally rotated shoulder
    • Extended elbow
    • Flexed wrist facing backward
    • Lack of movement in the affected arm
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31
Q

what is the prognosis for erbs palsy

A

usually resolves spontaneously within a few months

may require neuro surg input

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32
Q

what is a fractured clavicle associated with?

A

shoulder dystocia, traumatic/instrumental delivery, large birth weight

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33
Q

how does a fractures clavicle present?

A
  • Noticeable lack of movement or asymmetry of movement in affected arm
  • Asymmetry of the shoulders, with affected shoulder lower than the normal shoulder
  • Pain and distress on movement of the arm
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34
Q

how is a fractured clavicle conformed and managed?

A

Confirmed w/ USS or XR.

Management conservative, occasionally with immobilisation of the affected arm. It usually heals well.

Main complication of a clavicle is injury to the branchial plexus, with subsequent nerve palsy.

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35
Q

what is neonatal sepsis?

A

caused by infection in the neonatal period - potentially fatal

presents with very non specific signs

low threshold for starting broad spec abx

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36
Q

what are some common organisms in neonatal sepsis?

A

group B streptococcus

Escherichia coli

Listeria, Klebsiella

Staphylococcus aureus

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37
Q

what are some clinical features of neonatal sepsis?

A
  • Fever
  • Reduced tone and activity
  • Poor feeding
  • Respiratory distress or apnoea
  • Vomiting
  • Tachycardia or bradycardia
  • Hypoxia
  • Jaundice within 24H
  • Seizures
  • Hypoglycaemia
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38
Q

what are some red flags for neonatal sepsis?

A
  • Confirmed or suspected sepsis in mother
  • Signs of shock
  • Seizures
  • Term baby mechanical ventilation
  • Respiratory distress starting more than 4H after birth
  • Presumed sepsis in another baby in multiple pregnancy
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39
Q

how is neonatal sepsis treated?

A

local guidelines

  • Risk or clinical feature, monitor observations and clinical condition for at least 12H
  • 2+ risk factors or clinical features= start ABX
  • ABX start if single red flag
  • ABX should be given within 1H of making decision to start them
  • Blood cultures should be taken before abx given
  • Check baseline CRP and FBC
  • Perform LP if infection strongly suspected or there are features of meningitis
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40
Q

what antibiotics are given in neonatal sepsis?

A

benzylpenicillin and gentamycin

3rd gen cephalosporin given in lower risk babies

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41
Q

what ongoing management is required for neonatal sepsis?

A

Check CRP again at 24H and check the blood culture at 36H

Consider stopping abx if clinically well, the blood cultures are negative at 36H after taking them and both CRP<10

Check CRP at 5 days if still on treatment

Consider stopping abx if clinically well, LP and Blood cultures negative and CRP normal at 5 days.

Consider LP if any CRP>10

Urgent refer temp= <3/12 temp >38, 3-6/12 >39 or >5/7

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42
Q

what is hypoxic-ischaemic encephalopathy?

A

occurs in neonates as a result of hypoxia during birth.

Hypoxia is a lack of oxygen

ischaemia refers to a restriction in blood flow to the brain

encephalopathy refers to malfunctioning of the brain.

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43
Q

is hypoxia normal in childbirth?

A

Some hypoxia is normal during birth, however prolonged or severe hypoxia leads to ischaemic brain damage

HIE can lead to permanent damage to the brain, causing cerebral palsy. Severe can result in death.

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44
Q

when should HIE be suspected?

A

Suspected HIE in neonates when there are events that could lead to hypoxia during the perinatal or intrapartum period, acidosis (pH < 7) on the umbilical artery blood gas, poor Apgar scores, features of mild, moderate or severe HIE (see below) or evidence of multi organ failure.

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45
Q

anything that lead to asphyxia can cause HIE, what are some examples?

A
  • Maternal shock
  • Intrapartum haemorrhage
  • Prolapsed cord, causing compression of the cord during birth
  • Nuchal cord, where the cord is wrapped around the neck of the baby
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46
Q

what is the Hypoxic-Ischaemic Encephalopathy Grades (Sarnat Staging)?

A
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47
Q

how is HIE managed?

A

neonatal unit - supportive care with neonatal resuscitation and ongoing optimal ventilation, circulatory support, nutrition, acid base balance and treatment of seizures.

Therapeutic hypothermia - in some cases - to help protect the brain from hypoxic injury.

Children will need to be followed up by a paediatrician and the multidisciplinary team to assess their development and support any lasting disability.

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48
Q

what is Therapeutic Hypothermia?

A

Babies near or at term considered to have HIE can benefit from therapeutic hypothermia.

Involves actively cooling the core temperature of the baby according to a strict protocol.

transferred to neonatal ICU and actively cooled using cooling blankets and a cooling hat.

The temperature is carefully monitored with a target of between 33 and 34°C, measured using a rectal probe.

This is continued for 72 hours, after which the baby is gradually warmed to a normal temperature over 6 hours.

The intention of therapeutic hypothermia is to reduce the inflammation and neurone loss after the acute hypoxic injury.

reduces the risk of cerebral palsy, developmental delay, learning disability, blindness and death.

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49
Q

what is considered premature?

A

birth before 37 weeks

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50
Q

what is extreme prematureity?

A

under 28 weeks

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51
Q

what is very premature?

A

28-32 weeks

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52
Q

what is moderate to late preterm

A

32-37 weeks

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53
Q

when is resuscitation carefully considered in premature babies?

A

under 500g or less than 24 weeks

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54
Q

resuscitation preterm babys

A
  • Less than 23 weeks: not performed
  • 23 - 23+6 weeks may be decided not to intervene especially if wishes expressed by parents
  • 24 - 24+6 weeks commenced unless the baby is thought to be severely compromised
  • After 25 weeks resuscitate and start intensive care.
55
Q

what are some associations with prematurity? think social factors

A
  • Social deprivation
  • Smoking
  • Alcohol
  • Drugs
  • Overweight or underweight mother
  • Maternal co-morbidities
  • Twins
  • Personal or family history of prematurity
56
Q

what are the 2 options for trying to delay birth in women who have a cervical length of 25mm or less before 24 weeks gestation?

A
  • Prophylactic vaginal progesterone: putting a progesterone suppository in the vagina to discourage labour
  • Prophylactic cervical cerclage: putting a suture in the cervix to hold it closed
57
Q

what are some options for improving outcomes when preterm labour is suspected?

A
  • Tocolysis with nifedipine: nifedipine is a calcium channel blocker that suppresses labour
  • Maternal corticosteroids: can be offered before 35 weeks gestation to reduce neonatal morbidity and mortality
  • IV Magnesium sulphate: can be offered before 34 weeks gestation and helps protect the baby’s brain
  • Delayed cord clamping or cord milking: can increase the circulating blood volume and haemoglobin in the baby
58
Q

what are some issues preterm babies have in early life?

A
  • Respiratory distress syndrome
  • Hypothermia
  • Hypoglycaemia
  • Poor feeding
  • Apnoea and bradycardia
  • Neonatal jaundice
  • Intraventricular haemorrhage
  • Retinopathy of prematurity
  • Necrotising enterocolitis
  • Immature immune system and infection
59
Q

what are some long term effects of prematurity?

A
  • Chronic lung disease of prematurity (CLDP)
  • Learning and behavioural difficulties
  • Susceptibility to infections, particularly respiratory tract infections
  • Hearing and visual impairment
  • Cerebral palsy
60
Q

what is apnoea of prematurity?

A

Defined as periods where breathing stops spontaneously for more than 20 seconds, or shorter periods w/ oxygenation desaturation or bradycardia. Apnoea often followed by bradycardia.

Very common in premature neonates. Can occur in almost all babies <28/40 and incidence decreases w/ increased gestational age.

61
Q

what does it mean if a term baby has apnoeas?

A

underlying pathology

62
Q

what causes apnoea of prematurity?

A

Immaturity of the autonomic nervous system that controls respiration and HR. More immature in premature neonates.

  • Infection
  • Anaemia
  • Airway obstruction (may be positional)
  • CNS pathology- seizure or haemorrhage
  • GORD
  • Neonatal abstinence syndrome
63
Q

how is apnoea of prematurity managed?

A

Neonatal units attach apnoea monitors. They make a sound when an apnoea is occurring. Tactile stimulation is used to prompt the baby to restart breathing.

IV caffeine can be used to prevent apnoea and bradycardia in babies with recurrent episodes.

Episodes will settle as the baby grows and develops.

64
Q

what is retinopathy of prematurity?

A

Abnormal development of the blood vessels in the retina can lead to scarring, retinal detachment and blindness. Treatment can prevent blindness, which is why screening is so important.

usually affects preterm and low weight babies - typically <32 weeks gestation

65
Q

describe the development of the blood vessels in the retina of a newborn?

A

Retinal blood vessel development starts at around 16 weeks and is complete by 37-40 weeks. Blood vessels grow from the middle of the retina to the outer area. Vessel formation stimulated by hypoxia= normal for pregnancy.

66
Q

what happens to the retinal vessels development when newborns are exposed to higher oxygen concentrations?

A

When exposed to higher O2 concentration in preterm = stimulation for normal blood vessel development lost.

When hypoxic environment recurs, the retina responds by neovascularisation as well as scar tissue.

These abnormal vessels may regress and leave the retina w/o a blood supply.

Scar tissue may cause retinal detachment.

67
Q

how is the retina divided into zones for assessment?

A
  • Zone 1 includes the optic nerve and the macula
  • Zone 2 is from the edge of zone 1 to the ora serrata, the pigmented border between the retina and ciliary body
  • Zone 3 is outside the ora serrata

retinal areas are described as a clockface and diseases described in stages

68
Q

what is meant by plus disease when talking about ROP

A

“Plus disease” describes additional findings, such as tortuous vessels and hazy vitreous humour.

69
Q

who is screened for ROP and when is it done? when does it stop?

A

babies born before 32 weeks or under 1.5kg

born before 27 weeks = starts at 30-31 weeks gestational age

born after 27 weeks = 4-5 weeks of age

happens every 2 weeks and can cease when retinal vessels enter zone 3 - around 36 weeks gestation

70
Q

what is looked for on examination?

A

all retinal areas need to be visualised

monitor retinal vessels looking for plus disease

71
Q

what is the treatment for retinopathy of prematurity?

A

systematically targeting areas of the retina to stop new blood vessels developing

1st line = transpupilary laser photocoagulation to halt and reverse neovascularisation

alt = cryotherapy and injections of intravitreal VEGF inhibitors, surgery if retinal detachment

72
Q

what is respiratory distress syndrome and who does it affect?

A

affects premature neonates born before the lungs start producing adequate surfactant

commonly occurs below 32 weeks

73
Q

what does a CXR for respiratory distress syndrome show?

A

ground glass appearance

74
Q

what is the pathophysiology of respiratory distress syndrome?

A

Inadequate surfactant leads to high surface tension within alveoli. This leads to atelectasis (lung collapse), as it is more difficult for the alveoli and the lungs to expand. This leads to inadequate gaseous exchange, resulting in hypoxia, hypercapnia (high CO2) and respiratory distress.

75
Q

what is given to mothers in preterm labour to increase the production of surfactant and reduce the incidence and severity of respiratory distress syndrome?

A

dexamethasone

76
Q

how is respiratory distress syndrome managed?

A
  • Intubation and ventilation to fully assist breathing if the respiratory distress is severe
  • Endotracheal surfactant, which is artificial surfactant delivered into the lungs via an endotracheal tube
  • Continuous positive airway pressure (CPAP) via a nasal mask to help keep the lungs inflated whilst breathing
  • Supplementary oxygen to maintain oxygen saturations between 91 and 95% in preterm neonates
77
Q

what are some short term complications of respiratory distress syndrome?

A
  • Pneumothorax
  • Infection
  • Apnoea
  • Intraventricular haemorrhage
  • Pulmonary haemorrhage
  • Necrotising enterocolitis
78
Q

what are some long term complications of respiratory distress syndrome?

A
  • Chronic lung disease of prematurity
  • Retinopathy of prematurity occurs more often and more severely in neonates with RD
  • Neurological, hearing and visual impairment
79
Q

what is necrotising enterocolitis?

A

disorder affecting the premature neonates where part of the bowel becomes necrotic

life threatening emergency - death of bowel can cause perforation leading to peritonitis and shock

80
Q

what are some risk factors for developing NEC?

A
  • Very low birth weight or very premature
  • Formula feeds (it is less common in babies fed by breast milk feeds)
  • Respiratory distress and assisted ventilation
  • Sepsis
  • Patient ductus arteriosus and other congenital heart disease
81
Q

how does NEC present?

A
  • Intolerance to feeds
  • Vomiting, particularly with green bile
  • Generally unwell
  • Distended, tender abdomen
  • Absent bowel sounds
  • Blood in stools

when peritonitis - shock and ++ unwell

82
Q

what investigations are done for NEC?

A

Blood tests:

  • FBC - for thrombocytopenia and neutropenia
  • CRP for inflammation
  • Capillary blood gas will show a metabolic acidosis
  • Blood culture for sepsis

Abdominal xray is the investigation of choice for diagnosis. This is done front on in the supine position (lying face up). Additional views can be helpful, such as lateral (from the side with the patient on their back) and lateral decubitus (from the side with the neonate on their side).

83
Q

what can the abdo x rays show in NEC?

A
  • Dilated loops of bowel
  • Bowel wall oedema (thickened bowel walls)
  • Pneumatosis intestinalis is gas in the bowel wall and is a sign of NEC
  • Pneumoperitoneum is free gas in the peritoneal cavity and indicates perforation
  • Gas in the portal veins
84
Q

how is NEC managed?

A

NBM

IVF

TPN

ABX

NGT

Surgical input - may be required to removed dead bowel

85
Q

what are some complications of NEC?

A
  • Perforation and peritonitis
  • Sepsis
  • Death
  • Strictures
  • Abscess formation
  • Recurrence
  • Long term stoma
  • Short bowel syndrome after surgery
86
Q

what is neonatal abstinence syndrome?

A

withdrawal symptoms that happens in neonates of mothers that used substances in pregnancy

87
Q

what are some substances that cause neonatal abstinence syndrome?

A
  • Opiates
  • Methadone
  • Benzodiazepines
  • Cocaine
  • Amphetamines
  • Nicotine or cannabis
  • Alcohol
  • SSRI antidepressants
88
Q

when does withdrawal from opiates, diazepam, SSRI and alcohol usually occur?

A

between 3 and 72 hours after birth

89
Q

when does withdrawal from methadone and other benzodiazepines occur?

A

Between 24 and 21 days

90
Q

what are some CNS signs of withdrawal?

A
  • Irritability
  • Increased tone
  • High pitched cry
  • Not settling
  • Tremors
  • Seizures
91
Q

what are some vasomotor and respiratory signs of withdrawal?

A
  • Yawning
  • Sweating
  • Unstable temperature and pyrexia
  • Tachypnoea (fast breathing)
92
Q

what are some metabolic and gastrointestinal signs of withdrawal?

A
  • Poor feeding
  • Regurgitation or vomiting
  • Hypoglycaemia
  • Loose stools with a sore nappy area
93
Q

how is NAS managed?

A

mothers known to be substance uses should have alert in notes so neonate can have extra monitoring

monitor on NAS chart for at least 3 days

urine sample to test for substances

medical treatment for mod-severe symptoms with oral morphine sulphate for opiate withdrawal and oral phenobarbitone for non-opiate withdrawal

may need to be gradually weaned off substances

94
Q

what are some additional things to consider when managing NAS?

A
  • Testing for hepatitis B and C and HIV
  • Safeguarding and social service involvement
  • Safety-net advice for readmission if withdrawal signs and symptoms occur
  • Follow up from paediatrics, social services, health visitors and the GP
  • Support for the mother to stop using substances
  • Check the suitability for breastfeeding in mothers with substance use
95
Q

what is fetal alcohol syndrome?

A

certain effects and characteristics that are found in children of mothers that consumed significant alcohol during pregnancy

Alcohol in pregnancy can cross the placenta and enter the fetus and disrupts fetal development.

There is no safe level of alcohol in pregnancy and mothers are encouraged not to drink alcohol at all, however small amounts are less likely to result in lasting effects.

The effects are greatest in the first 3 months of pregnancy.

96
Q

what are the 3 things that Alcohol in early pregnancy can lead to?

A
  • Miscarriage
  • Small for dates
  • Preterm delivery
97
Q

what are some features of fetal alcohol syndrome?

A
  • Microcephaly (small head)
  • Thin upper lip
  • Smooth flat philtrum (the groove between the nose and upper lip)
  • Short palpebral fissure (short horizontal distance from one side of the eye and the other)
  • Learning disability
  • Behavioural difficulties
  • Hearing and vision problems
  • Cerebral palsy
98
Q

how is fetal alcohol syndrome managed?

A

irreversible damage to child’s brain and body

99
Q

what is sudden infant death syndrome?

A

sudden unexplained death in an infant

aka cot death - usually occurs in first 6 months of life

100
Q

what are some risk factors for SIDS?

A
  • Prematurity
  • Low birth weight
  • Smoking during pregnancy
  • Male baby (only slightly increased risk)
101
Q

how can the risk of SIDS be reduced?

A
  • Put the baby on their back when not directly supervised
  • Keep their head uncovered
  • Place their feet at the foot of the bed to prevent them sliding down and under the blanket
  • Keep the cot clear of lots of toys and blankets
  • Maintain a comfortable room temperature (16 – 20 ºC)
  • Avoid smoking. Avoid handling the baby after smoking (smoke stays on clothes).
  • Avoid co-sleeping, particularly on a sofa or chair
  • If co-sleeping avoid alcohol, drugs, smoking, sleeping tablets or deep sleepers
102
Q

what support is available for parents affected by SIDS?

A

lullaby trust - charity, offers counselling to affected families

Care of next infant - CONI - supports parents with next infant after a SIDS, provides extra home support, visits, resuscitation training and access to equipment to monitor babys movements and alarms if stops breathing

103
Q

what is neonatal jaundice?

A

abnormally high levels of bilirubin in the blood

104
Q

describe the usual excretion of bilirubin

A

Red blood cells contain unconjugated bilirubin. When red blood cells break down, they release unconjugated bilirubin into the blood. Unconjugated bilirubin is conjugated in the liver. Conjugated bilirubin is excreted in two ways: via the biliary system into the gastrointestinal tract and via the urine.

105
Q

what is physiological jaundice?

A

high conc of RBC in fetus and neonate which are more fragile than normal RBC and they have less well developed liver function

fetal RBC break down more rapidly that normal RBC releasing ++ bilirubin and as the fetus no longer has access to placenta to excrete it, leads to normal rise in bilirubin shortly after birth

106
Q

when does a baby with physiological jaundice start to become visibly jaundice?

A

mild yellowing of skin and sclera from 2 – 7 days of age

usually resolves completely by 10 days

most remain healthy and well

107
Q

what are some causes of neonatal jaundice due to increased production of bilirubin?

A
  • Haemolytic disease of the newborn
  • ABO incompatibility
  • Haemorrhage
  • Intraventricular haemorrhage
  • Cephalo-haematoma
  • Polycythaemia
  • Sepsis and disseminated intravascular coagulation
  • G6PD deficiency
108
Q

what are some causes of neonatal jaundice due to decreased clearance of bilirubin?Prematurity

A
  • Prematurity
  • Breast milk jaundice
  • Neonatal cholestasis
  • Extrahepatic biliary atresia
  • Endocrine disorders (hypothyroid and hypopituitary)
  • Gilbert syndrome
109
Q

what is significant about jaundice in the 1st 24 hours of life?

A

it is pathological!

may be sepsis

110
Q

what is jaundice in premature neonates?

A

process of physiological jaundice is exaggerated due to immature liver increasing risk of complications - kernicterus

111
Q

what is breast milk jaundice?

A

babies breastfed = more likely to be jaundiced

several reasons

  • components of breast milk inhibit ability of liver to process bilirubin
  • more likely to become dehydrated if not feeding adequately = slow passage of stools & increasing absorption of bilirubin in intestines

breastfeeding should be encouraged as benefits outweigh the risks

112
Q

what is haemolytic disease of the newborn?

A

it is a cause of haemolysis and jaundice in the neonate caused by incompatibility between the rhesus antigens on the surface of the red blood cells of the mother and fetus.

most important antigen in the rhesus blood group system is rhesus D antigen

when a woman is rhesus D negative, she may have a rhesus positive child and at some point during the pregnancy her blood may mix with her childs at which point the babys rbc will display rhesus d antigen. mothers body will then produce antibodies to rhesus D antigen and the mother will become sensitised to rhesus D antigens

Doesn’t usually cause problems in 1st pregnancy but if second child is rhesus positive - mothers antibodies can cross placenta and attatch to fetus RBC. immune system of fetus then attacks their own RBC = haemolysis = anaemia and high bilirubin levels

113
Q

what is considered to be prolonged jaundice?

A
  • More than 14 days in full term babies
  • More than 21 days in premature babies
114
Q

what needs to be done when a fetus is jaundiced for a prolonged period of time?

A

further investigation to look for underlying cause such as biliary atresia, hypothyroidism, G6PD deficiency

115
Q

what investigations are done for a jaundiced baby?

A
  • FBC and blood film - polycythaemia or anaemia
  • Conjugated bilirubin: elevated levels indicate a hepatobiliary cause
  • Blood type testing of mother and baby for ABO or rhesus incompatibility
  • Direct Coombs Test (direct antiglobulin test) for haemolysis
  • Thyroid function, particularly for hypothyroid
  • Blood and urine cultures if infection is suspected. Suspected sepsis needs treatment with antibiotics.
  • Glucose-6-phosphate-dehydrogenase (G6PD) levels for G6PD deficiency
116
Q

how is jaundice managed?

A

total bilirubin levels are monitored and plotted on treatment threshold charts specific to gestational age of baby

if bilirubin levels reach threshold - commence treatment

Phototherapy usually adequate but extremely high levels may require exchange transfusion

117
Q

what is phototherapy?

A

converts unconjugated bilirubin into isomers that can be excreted in bile and urine without requiring conjugation in the liver

baby placed under blue light in nappy with eye patches

monitor bilirubin throughout

once phototherapy is complete a rebound bilirubin should be measured 12-18 hours after stopping to ensure the levels do not rise again

118
Q

what is kernicterus?

A

type of brain damage caused by excessive bilirubin levels - main reason we treat neonatal jaundice to keep bilirubin levels below certain thresholds

Bilirubin can cross bbb - excessive bilirubin causes direct damage to CNS

119
Q

how does kernicterus present?

A

less responsive, floppy, drowsy baby with poor feeding

120
Q

what is the long term implication of kernicterus?

A

damage to the nervous system is permeant, causing cerebral palsy, learning disability and deafness. Kernicterus is now rare due to effective treatment of jaundice.

121
Q

what is meconium aspiration syndrome?

A

Meconium aspiration is when a newborn breathes in a mixture of meconium and amniotic fluid. Meconium is the baby’s first stool.

122
Q

what are some risk factors for meconium aspiration syndrome?

A

Post-term babies, foetal distress, intrapartum hypoxia secondary to placental insufficiency, APGAR>7, Oligohydramnios, Maternal HTN, Pre-eclampsia, maternal smoking, maternal substance abuse

123
Q

how does meconium aspiration syndrome present?

A

Meconium aspiration can present with respiratory distress and staining of the newborn skin.

124
Q

what investigations are done for meconium aspiration syndrome?

A
  • CXR- increased lung volumes, asymmetrical patchy pulmonary opacities, pleural effusions, pneumothorax, multifocal consolidation
  • Infection markers- FBC, CRP, blood cultures
  • ABG
  • Dual pulse oximetry
  • ECHO
  • Cranial USS
125
Q

what are the complications of meconium aspiration syndrome?

A
  • Airway obstruction/collapse
  • Surfactant dysfunction
  • Pulmonary vasoconstriction
  • Chemical pneumonitis
  • Aspiration pneumonia
126
Q

how is meconium aspiration syndrome managed?

A
  • Surfactant replacement
  • Ventilation
  • Antibiotics
  • Observation
  • Inhaled NO2
  • Corticosteroids
127
Q

what is persistent pulmonary HTN of the newborn?

A

Hypoxia acts to keep the ductus arteriosus open, and thus maintain fetal circulation. Hypoxia also causes vasoconstriction of the PA, therefore increasing pulmonary HTN.

128
Q

what are some risk factors for persistent pulmonary HTN of the newborn?

A

hypoxia at delivery or birth, sepsis, polycythaemia, maternal diabetes, meconium aspiration

129
Q

what are the clinical features of persistent pulmonary HTN of the newborn?

A
  • Cyanosis
  • Tachypnoea
130
Q

what investigations need to be done for persistent pulmonary HTN of the newborn?

A
  • Sepsis Screen
  • CXR
  • Blds
  • ECHO
  • Cranial USS (when considering ECMO)
131
Q

how is persistent pulmonary HTN of the newborn managed?

A
  • Supportive measures- including ventilation
  • Prostacyclin infusion
  • ECMO
132
Q

what are some causes of infant feeding problems?

A

Candida Albicans

Colic

Cow’s milk protein allergy

lactose intolerance

GORD

133
Q

how do infant feeding problems present?

A

Episodes of irritability, fussing, or crying that begin and end for no apparent reason, and last 3 or more hours per day, 3 or more days a week and 1 or more weeks.

  • Inconsolable crying
  • Redness of the face
  • Drawing up of the knees
  • Flatus
134
Q

how to manage infant feeding problems

A
  • Reassure that colic usually resolves by 4 months
  • Hold the baby through crying
  • White noise
  • Bathing in warm water
  • Hypoallergenic diet
  • Simethicone drops